Nitric oxide scavenger carboxy-PTIO reduces infarct volume following permanent focal ischemia

Shih Yuan Fang, Chia Chih Tseng, Yao Lin Yang, E. Jian Lee, Hung Yi Chen, Anish Bhardwaj, Tsung Ying Chen

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Background: Nitric oxide (NO) has been shown to play a dual role as a neuroprotectant and a neurotoxin in cerebral ischemia. Free radical scavengers protect brain tissue from ischemic injury. Consequently, we examined the neuroprotective action of NO scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (carboxy-PTIO), in cerebral ischemia induced by permanent middle cerebral artery occlusion (MCAO) in rats and mice. Methods: All experiments were performed in a randomized fashion. In the first series of experiments, adult Sprague-Dawley rats (n = 31) subjected to permanent MCAO were treated with carboxy-PTIO (0.3, 0.6 mg/ kg) or vehicle (normal saline) injected intraperitoneally (IP) 1 hr before permanent MCAO. In the second series of experiments, adult C57BL/ 6NCrj mice (n = 49) were treated with carboxy-PTIO (0.6, 1.2 mg/kg) or vehicle saline 30 min following MCAO. Neurobehavioral scores were determined 22-24 hr following permanent MCAO and infarct volumes determined by quantitative image analysis of 2, 3, 5-triphenyltetrazolium (TTC)-stained brain sections. Results: Pre-treatment with carboxy-PTIO at 0.6 mg/kg IP in rats significantly attenuated infarct volume (19.9 ± 2.9%; n = 10) as compared with vehicle-treated controls (29.2 ± 2.7%; n = 16), but not at 0.3 mg/kg (28.3 ± 8.4%; n = 5). Post-MCAO treatment in mice with 0.6 mg/kg carboxy-PTIO (30.3 ± 3.9%; n = 16) significantly attenuated infarct volume as compared with vehicle-treated controls (46.1 ± 2.8%; n = 18). Conclusions: These data demonstrate that NO scavenger, carboxy-PTIO, provides significant ischemic neuroprotection when given as a pre-treatment as well as after the onset of permanent focal ischemia in two animal species.

Original languageEnglish (US)
Pages (from-to)141-146
Number of pages6
JournalActa Anaesthesiologica Taiwanica
Volume44
Issue number3
StatePublished - Sep 2006
Externally publishedYes

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Middle Cerebral Artery Infarction
Nitric Oxide
Ischemia
Brain Ischemia
Free Radical Scavengers
Neurotoxins
Brain
Neuroprotective Agents
1,3-dihydroxy-4,4,5,5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole
Inbred C57BL Mouse
Sprague Dawley Rats
Wounds and Injuries

Keywords

  • Brain ischemia
  • Free radical scavengers
  • Neuroprotective agents
  • Nitric oxide

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

Cite this

Fang, S. Y., Tseng, C. C., Yang, Y. L., Lee, E. J., Chen, H. Y., Bhardwaj, A., & Chen, T. Y. (2006). Nitric oxide scavenger carboxy-PTIO reduces infarct volume following permanent focal ischemia. Acta Anaesthesiologica Taiwanica, 44(3), 141-146.

Nitric oxide scavenger carboxy-PTIO reduces infarct volume following permanent focal ischemia. / Fang, Shih Yuan; Tseng, Chia Chih; Yang, Yao Lin; Lee, E. Jian; Chen, Hung Yi; Bhardwaj, Anish; Chen, Tsung Ying.

In: Acta Anaesthesiologica Taiwanica, Vol. 44, No. 3, 09.2006, p. 141-146.

Research output: Contribution to journalArticle

Fang, SY, Tseng, CC, Yang, YL, Lee, EJ, Chen, HY, Bhardwaj, A & Chen, TY 2006, 'Nitric oxide scavenger carboxy-PTIO reduces infarct volume following permanent focal ischemia', Acta Anaesthesiologica Taiwanica, vol. 44, no. 3, pp. 141-146.
Fang, Shih Yuan ; Tseng, Chia Chih ; Yang, Yao Lin ; Lee, E. Jian ; Chen, Hung Yi ; Bhardwaj, Anish ; Chen, Tsung Ying. / Nitric oxide scavenger carboxy-PTIO reduces infarct volume following permanent focal ischemia. In: Acta Anaesthesiologica Taiwanica. 2006 ; Vol. 44, No. 3. pp. 141-146.
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abstract = "Background: Nitric oxide (NO) has been shown to play a dual role as a neuroprotectant and a neurotoxin in cerebral ischemia. Free radical scavengers protect brain tissue from ischemic injury. Consequently, we examined the neuroprotective action of NO scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (carboxy-PTIO), in cerebral ischemia induced by permanent middle cerebral artery occlusion (MCAO) in rats and mice. Methods: All experiments were performed in a randomized fashion. In the first series of experiments, adult Sprague-Dawley rats (n = 31) subjected to permanent MCAO were treated with carboxy-PTIO (0.3, 0.6 mg/ kg) or vehicle (normal saline) injected intraperitoneally (IP) 1 hr before permanent MCAO. In the second series of experiments, adult C57BL/ 6NCrj mice (n = 49) were treated with carboxy-PTIO (0.6, 1.2 mg/kg) or vehicle saline 30 min following MCAO. Neurobehavioral scores were determined 22-24 hr following permanent MCAO and infarct volumes determined by quantitative image analysis of 2, 3, 5-triphenyltetrazolium (TTC)-stained brain sections. Results: Pre-treatment with carboxy-PTIO at 0.6 mg/kg IP in rats significantly attenuated infarct volume (19.9 ± 2.9{\%}; n = 10) as compared with vehicle-treated controls (29.2 ± 2.7{\%}; n = 16), but not at 0.3 mg/kg (28.3 ± 8.4{\%}; n = 5). Post-MCAO treatment in mice with 0.6 mg/kg carboxy-PTIO (30.3 ± 3.9{\%}; n = 16) significantly attenuated infarct volume as compared with vehicle-treated controls (46.1 ± 2.8{\%}; n = 18). Conclusions: These data demonstrate that NO scavenger, carboxy-PTIO, provides significant ischemic neuroprotection when given as a pre-treatment as well as after the onset of permanent focal ischemia in two animal species.",
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AU - Fang, Shih Yuan

AU - Tseng, Chia Chih

AU - Yang, Yao Lin

AU - Lee, E. Jian

AU - Chen, Hung Yi

AU - Bhardwaj, Anish

AU - Chen, Tsung Ying

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N2 - Background: Nitric oxide (NO) has been shown to play a dual role as a neuroprotectant and a neurotoxin in cerebral ischemia. Free radical scavengers protect brain tissue from ischemic injury. Consequently, we examined the neuroprotective action of NO scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (carboxy-PTIO), in cerebral ischemia induced by permanent middle cerebral artery occlusion (MCAO) in rats and mice. Methods: All experiments were performed in a randomized fashion. In the first series of experiments, adult Sprague-Dawley rats (n = 31) subjected to permanent MCAO were treated with carboxy-PTIO (0.3, 0.6 mg/ kg) or vehicle (normal saline) injected intraperitoneally (IP) 1 hr before permanent MCAO. In the second series of experiments, adult C57BL/ 6NCrj mice (n = 49) were treated with carboxy-PTIO (0.6, 1.2 mg/kg) or vehicle saline 30 min following MCAO. Neurobehavioral scores were determined 22-24 hr following permanent MCAO and infarct volumes determined by quantitative image analysis of 2, 3, 5-triphenyltetrazolium (TTC)-stained brain sections. Results: Pre-treatment with carboxy-PTIO at 0.6 mg/kg IP in rats significantly attenuated infarct volume (19.9 ± 2.9%; n = 10) as compared with vehicle-treated controls (29.2 ± 2.7%; n = 16), but not at 0.3 mg/kg (28.3 ± 8.4%; n = 5). Post-MCAO treatment in mice with 0.6 mg/kg carboxy-PTIO (30.3 ± 3.9%; n = 16) significantly attenuated infarct volume as compared with vehicle-treated controls (46.1 ± 2.8%; n = 18). Conclusions: These data demonstrate that NO scavenger, carboxy-PTIO, provides significant ischemic neuroprotection when given as a pre-treatment as well as after the onset of permanent focal ischemia in two animal species.

AB - Background: Nitric oxide (NO) has been shown to play a dual role as a neuroprotectant and a neurotoxin in cerebral ischemia. Free radical scavengers protect brain tissue from ischemic injury. Consequently, we examined the neuroprotective action of NO scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (carboxy-PTIO), in cerebral ischemia induced by permanent middle cerebral artery occlusion (MCAO) in rats and mice. Methods: All experiments were performed in a randomized fashion. In the first series of experiments, adult Sprague-Dawley rats (n = 31) subjected to permanent MCAO were treated with carboxy-PTIO (0.3, 0.6 mg/ kg) or vehicle (normal saline) injected intraperitoneally (IP) 1 hr before permanent MCAO. In the second series of experiments, adult C57BL/ 6NCrj mice (n = 49) were treated with carboxy-PTIO (0.6, 1.2 mg/kg) or vehicle saline 30 min following MCAO. Neurobehavioral scores were determined 22-24 hr following permanent MCAO and infarct volumes determined by quantitative image analysis of 2, 3, 5-triphenyltetrazolium (TTC)-stained brain sections. Results: Pre-treatment with carboxy-PTIO at 0.6 mg/kg IP in rats significantly attenuated infarct volume (19.9 ± 2.9%; n = 10) as compared with vehicle-treated controls (29.2 ± 2.7%; n = 16), but not at 0.3 mg/kg (28.3 ± 8.4%; n = 5). Post-MCAO treatment in mice with 0.6 mg/kg carboxy-PTIO (30.3 ± 3.9%; n = 16) significantly attenuated infarct volume as compared with vehicle-treated controls (46.1 ± 2.8%; n = 18). Conclusions: These data demonstrate that NO scavenger, carboxy-PTIO, provides significant ischemic neuroprotection when given as a pre-treatment as well as after the onset of permanent focal ischemia in two animal species.

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